Endotheliopathy and Platelet Dysfunction as Hallmarks of Fatal Lassa Fever
Lucy E. Horton
1, Robert W. Cross
1, Jessica N. Hartnett, Emily J. Engel, Saori Sakabe, Augustine Goba, Mambu Momoh, John Demby Sandi, Thomas W. Geisbert, Robert F. Garry, John S. Schieffelin, Donald S. Grant, and Brian M. Sullivan
Author affiliations: The Scripps Research Institute, La Jolla, California, USA (L.E. Horton, S. Sakabe, B.M. Sullivan); University of Texas Medical Brach, Galveston, Texas, USA (R.W. Cross, T.W. Geisbert); Tulane University School of Medicine, New Orleans, Louisiana, USA (J.N. Hartnett, E.J. Engel, R.F. Garry, J.S. Schieffelin); Kenema Government Hospital, Kenema, Sierra Leone (A. Goba, M. Momoh, J.D. Sandi, D.S. Grant); Ministry of Health and Sanitation, Freetown, Sierra Leone (A. Goba, M. Momoh, J.D. Sandi); Eastern Polytechnic Institute, Kenema (M. Momoh, D.S. Grant); Njala University, Moyamba, Sierra Leone (J.D. Sandi); University of Sierra Leone, Freetown (D.S. Grant)
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Figure 5
Figure 5. Soluble endothelial protein C receptor plasma levels in patients with acute LF, NLFCs, and HCs, Sierra Leone, 2015–2018. A) EPCR is not statistically significantly different across groups (Kruskal-Wallis p = 0.0889). Error bars show SDs; horizontal lines indicate means. B) EPCR plasma levels correlated with soluble thrombomodulin in patients with acute LF. Patients with higher levels of soluble THBD tended to have higher levels of EPCR (n = 19). When analyzed by survival, a statistically significant positive correlation was found only in fatal LF cases (n = 9). Dashed lines and gray shading indicate limits of detection. D, died; EPCR, endothelial protein C receptor; HC, healthy control; LF, Lassa fever; NLFC, non-LF fever febrile control; THBD, thrombomodulin.
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